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J. Biol. Chem., Vol. 278, Issue 26, 23672-23677, June 27, 2003

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CD98 and Intracellular Adhesion Molecule I Regulate the Activity of Amino Acid Transporter LAT-2 in Polarized Intestinal Epithelia^*

Xia Liu , Laetitia Charrier , Andrew Gewirtz , Shanthi Sitaraman  and Didier Merlin  ¶

From the Department of Medicine, Division of Digestive Diseases and the Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, Georgia 30322

We have previously shown that the heterodimer CD98/LAT-2 (LAT-2: amino acid transporter) is expressed in the basolateral membrane of intestinal epithelia and is associated with ₁ integrin (Merlin, D., Sitaraman, S., Liu, X., Easterburn, K., Sun, J., Kucharzik, T., Lewis, B., and Madara, J. L. (2001) J. Biol. Chem. 276, 39282–39289). In the present study we examined the interaction of CD98/LAT2 with intracellular adhesion molecule I (ICAM-1) and the potential of such interaction on the activation of intracellular signal in Caco2-BBE cell monolayers. ICAM-1 was found to be expressed to the basolateral domain and to selectively coimmunoprecipitate with CD98/LAT-2 in Caco2-BBE monolayers. Using antibodies as ligands to CD98 and ICAM-1, we demonstrate that the basolateral cross-linking of CD98 and ICAM-1 differentially affects the intrinsic activity of the LAT-2 transporter. Whereas CD98 ligation decreases the K_m and V_m of the LAT-2 transporter, ICAM-1 ligation increases K_m and V_m of the amino acid transporter LAT-2. In addition, basolateral cross-linking of CD98 or ICAM-1 induces threonine phosphorylation of an 160-kDa supramolecular complex that is consistent with CD98/LAT-2-ICAM-1 complex. Together these findings demonstrate that (i) CD98/LAT-2 interacts with ICAM-1 in Caco2-BBE cell monolayers, and (ii) CD98 and ICAM-1 ligands generate intracellular signals that regulate the amino acids transporter (LAT-2) activity. Our data provide a novel mechanism by which events such as adhesion may be integrated by amino acid transport activity resulting from the direct interaction of cell surface molecules such as CD98 and ICAM-1.

Received for publication, March 18, 2003

^* This work was supported by National Institutes of Health Grants DK-02831 (to D. M.) and DK-02802 (to S. S.) and a Senior Research Award from the Crohn's and Colitis Foundation of America (to D. M.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

^¶ To whom correspondence should be addressed: Emory University, Dept. of Medicine, Division of Digestive Diseases, 615 Michael St., Atlanta, GA 30322. Tel.: 404-727-6454; Fax: 419-821-3041; E-mail: dmerlin{at}emory.edu.

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